Central Toxic Keratopathy

From EyeWiki
Original article contributed by: Majid Moshirfar, M.D., Ribhi Hazin, M.D.
All contributors: Brad H. Feldman, M.D. and Majid Moshirfar, M.D.
Assigned editor:
Review: Assigned status Update Pending by Natalie Afshari, MD FACS on January 19, 2015.


Central toxic keratopathy (CTK) describes a rare, acute, non-inflammatory complication of laser assisted in situ keratomileusis (LASIK) surgery. Fraenkel and colleagues first described CTK in 1989 as being inflammatory in nature but the condition has subsequently been recognized as a non-inflammatory process.


Although the exact cause of CTK is ambiguous [1][2], a number theories abound regarding possible factors contributing to the development of CTK. Among the most prominent suggestions in the literature are photoactivation of povidone-iodine by the excimer laser, laser-induced keratocyte apoptosis of corneal matrix [2], intraoperative exposure to meibomian gland secretions [2], marking pen ink [3], talc from latex surgical gloves [1], or post-surgical debris from the microkeratome blade [1].


The characteristic clinical appearance in CTK bears a striking resemblance to a number of inflammatory and infectious conditions including contact lens-induced keratitis [4] [5], infectious keratitis [5], post-photorefractive keratectomy (PRK) haze[3], epithelial ingrowth, diffuse lamellar keratitis (DLK) [1][2], and corneal haze secondary to increased intraocular pressure [3].
Despite its shared features with other disease processes, CTK can be appropriately distinguished from masquerading conditions via a thorough history and an of awareness of timing of onset, existing inciting factors, and by the nature of clinical findings each disease characteristically exhibits.

For example, although both DLK and CTK both lead to a reduction in corneal clarity and a hyperopic shift, the post-surgical opacification seen in DLK tends to be nonlocalized [1] and subepithelial [3] while the post-surgical haze in CTK is centralized and extends anteriorly or posteriorly from the interface. Similarly, unlike infectious or inflammatory processes which exhibit characteristic features, CTK rarely presents with chamber reaction, conjunctival hyperemia, or ciliary flush [1].

Scheimpflug imaging and optical coherence tomography (OCT) imaging studies may offer diagnostic clues into CTK-specific corneal alterations. Specifically, Scheimpflug imaging is useful in highlighting the exaggerated flattening of the anterior cornea that commonly accompanies CTK [1]. Similarly, OCT images of eyes affected with CTK will typically demonstrate central corneal thinning, central backscattering, and higher internal reflectivity when compared to normal eyes [1].


Patients with CTK typically develop dense central corneal opacification, stromal tissue loss, striae, and significant hyperopic refractive shift [1][2]. These signs typically begin on post-operative day 2-6. The central corneal opacification in CTK begins as diffuse lamellar keratitis (DLK) on post-surgery day 1 or 2 and quickly gives rise to a dense opacification of the central corneal stroma [2]. This corneal opacity and hyperopic shift characteristically persists for 2-18 months before spontaneously resolving [1].


Common symptoms associated with CTK include photophobia, pain, floaters, redness, halos, and a hyperopic shift. CTK often leads to reduced best spectacle-corrected visual acuity (BSCVA) in affected patients [1][2].

Differential Diagnosis

  • Diffuse lamellar keratitis (DLK)
  • Infectious keratitis
  • Interface fluid
  • Corneal haze secondary to increased IOP
  • Superficial punctuate keratitis
  • Epithelial ingrowth
  • Trauma

Management and Follow up

Since the centralized stromal haze in CTK spontaneously resolves within 18 months without treatment, close monitoring and regularly-scheduled follow-up remains the primary management strategy in patients with CTK [1][3]. Although corticosteroids were used in the past, the recent discovery that CTK is non-inflammatory in nature coupled with the fact that CTK is unresponsive to steroid therapy have discouraged the use of these medications in the management of CTK[1][3].


Given its rarity and the fact that it shares striking similarities with other infectious and inflammatory processes, CTK is commonly mismanaged and misdiagnosed. CTK typically resolves spontaneously within 18 months with minimal complications or permanent sequelae [1][2]. Most complications, however, that arise in the setting of CTK typically occur as a result of mismanagement with steroids or other similar medications that can exacerbate preexisting refractive or anatomic alterations in this patient population [1].


The prognosis for CTK is excellent. In most cases, the condition resolves within 18 months of the inciting refractive procedure.

Additional Resources


  1. 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 Moshirfar M, Hazin R, Khalifa YM. Central Toxic Keratopahy after LASIK surgery. Current Opinion in Ophthalmology 2010 Jul;21(4):274-9.
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 Sonmez B, Maloney RK.Central toxic keratopathy: description of a syndrome in laser refractive surgery. Am J Ophthalmol 2007;143:420-7.
  3. 3.0 3.1 3.2 3.3 3.4 3.5 Hazin R, Daoud YJ, Khalifa YM. What is Central Toxic Keratopathy Syndrome if it is not Diffuse lamellar Keratitis Grade IV? Middle East Afr J Ophthalmol. 2010 Jan;17(1):60-2.
  4. Moshirfar M, Madsen M, Wolsey D. Re: central toxic keratopathy: description of a syndrome in laser refractive surgery. Am J Ophthalmol 2007;144:332; author reply 333-4.
  5. 5.0 5.1 Moshirfar M, Kurz C, Ghajarnia M. Contact lens-induced keratitis resembling central toxic keratopathy syndrome. Cornea 2009;28:1077-80.